Xiong Ye, Zhang Jing, Shi Lingzhi, Ning Yunye, Zhu Ying, Chen Si, Yang Meng, Chen Jingyu, Zhou Guo-Wu, Li Qiang
Department of Respiratory Medicine, Changhai Hospital, Second Military Medical University, Shanghai, China.
Department of Pathology, Changhai Hospital, Second Military Medical University, Shanghai, China.
Oncotarget. 2017 Aug 16;8(41):71024-71037. doi: 10.18632/oncotarget.20297. eCollection 2017 Sep 19.
Idiopathic pulmonary fibrosis (IPF) is a lung disease with an extremely poor prognosis. Epithelial mesenchymal transition (EMT) appearing on the airway epithelial cell plays an essential role in the formation and development of Idiopathic pulmonary fibrosis. In this paper, Bleomycin (BLM)-induced mice model combined with bioinformatics analysis were employed to elucidate the potential mechanism of EMT in pulmonary fibrosis. The obtained results showed that endoplasmic reticulum protein Nogo-b may promote MMP14-mediated proprotein maturation of TGF-β1, accelerating the release of free TGF-β1 in type II airway epithelial cells A549, subsquently, induce the epithelial-mesenchymal transition (EMT) of the cell. In all, the overexpression of Nogo-b play a role in the course of pulmonary fibrosis by influencing the EMT ability of cells.
特发性肺纤维化(IPF)是一种预后极差的肺部疾病。气道上皮细胞出现的上皮-间质转化(EMT)在特发性肺纤维化的形成和发展中起重要作用。本文采用博来霉素(BLM)诱导的小鼠模型并结合生物信息学分析,以阐明EMT在肺纤维化中的潜在机制。所得结果表明,内质网蛋白Nogo-b可能促进MMP14介导的TGF-β1前体蛋白成熟,加速II型气道上皮细胞A549中游离TGF-β1的释放,随后诱导细胞的上皮-间质转化(EMT)。总之,Nogo-b的过表达通过影响细胞的EMT能力在肺纤维化过程中发挥作用。